Tenascin‐C induced stimulation of chondrogenesis is dependent on the presence of the C‐terminal fibrinogen‐like globular domain

Murphy, Lyn I.; Fischer, Doris; Chiquet‐Ehrismann, Ruth; Mackie, Eleanor J.

doi:10.1016/s0014-5793(00)01936-0

Cited by 17 publications

(13 citation statements)

References 17 publications

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“…44 TNC has been shown previously to be associated with chondrogenic and osteogenic differentiation in vivo in chick embryos and has been shown to promote chondrogenesis in wing bud cultures of chick embryo in vitro. [45][46][47] However, in the presence of a proliferation medium, the mixed matrix of Col I and TNC neither induced osteogenic or adipogenic differentiation nor interfered with subsequent induction of these states. Most importantly, we found that the mixture of TNC and Col I protected MSCs from FasL-induced cell death, and that the effects of survival were due to TNC and not Col I.…”

Section: Discussionmentioning

confidence: 98%

The Matrikine Tenascin-C Protects Multipotential Stromal Cells/Mesenchymal Stem Cells from Death Cytokines Such as FasL

Rodrigues

Yates

Nuschke

et al. 2013

Tissue Engineering Part A

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Multipotential stromal cells/mesenchymal stem cells (MSCs) are attractive candidates for regenerative therapy due to the ability of these cells to differentiate and positively influence neighboring cells. However, on implantation for wound reconstruction, these cells are lost as they are challenged by nonspecific inflammation signals generated in the wound environment and in response to any implanted foreign body. We have previously shown that sustained and surface-restricted epidermal growth factor receptor (EGFR) signaling by a tethered form of its prototypal ligand EGF enhances survival of MSC in the presence of death cytokines such as FasL, serum deprivation, and low oxygen in vitro. This was proposed to be due to the plasma membrane restriction of EGFR signaling. Interestingly, during wound repair, an extracellular matrix (ECM) component Tenascin-C (TNC) containing EGF-like repeats (EGFL) and fibronectin-like repeats (FNL) is upregulated. A few of the 14 EGFL on each of the 6 arms, especially the 14th, bind as low-affinity/high-avidity ligands to EGFR causing sustained surface-restricted EGFR signaling. We queried whether signaling by this physiologically relevant EGFR matrikine also protects MSCs from FasLinduced death. MSCs grown on TNC and Collagen I (as TNC by itself is antiadhesive) displayed a survival advantage in the presence of FasL. TNC neither sequestered nor neutralized FasL; rather, the effects of survival were via cell signaling. This survival was dependent on TNC activating EGFR and downstream pathways of Erk and Akt through EGFL; to a much lesser extent, the FNL of TNC also contributed to survival. Taken together, these results suggest that providing MSCs with a nonimmunogenic naturally occurring ECM moiety such as TNC enhances their survival in the presence of death factors, and this advantage occurs via signaling through EGFR primarily and integrins only to a minor extent. This matrix component is proposed to supplement MSC delivery on the scaffolds to provide a survival advantage against death upon in vivo implantation.

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Section: Discussionmentioning

confidence: 98%

The Matrikine Tenascin-C Protects Multipotential Stromal Cells/Mesenchymal Stem Cells from Death Cytokines Such as FasL

Rodrigues

Yates

Nuschke

et al. 2013

Tissue Engineering Part A

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“…102,103 Additionally, the fibrinogen domain of TN-C plays a pivotal role in stimulating the proliferation of chondrocytes via the ERK/MAPK-pathway. 104 In contrast, the combination of all FNIII-domains decreases the proliferative effect of intact TN-C on glioma cells. 38 …”

Section: Tn-c In Tumor Cell Proliferationmentioning

confidence: 99%

Role of tenascins in the ECM of gliomas

Brösicke

Faissner

2015

Cell Adhesion & Migration

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“…Tenascin-C presumably interferes by binding both to fibronectin and to syndecan [41]. This would explain why the FNIII repeats as well as the (heparin-binding) fibrinogen-like domain of tenascin-C are required for full anti-spreading activity [43][44][45][46].…”

Section: Tenascins As Modulators Of Cell Adhesion Migration and Growthmentioning

confidence: 99%

Tenascins: regulation and putative functions during pathological stress

Chiquet‐Ehrismann

Chiquet

2003

The Journal of Pathology

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483

414

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In this review, we discuss the structure and function of the extracellular matrix protein family of tenascins with emphasis on their involvement in human pathologies. The article is divided into the following sections: Introduction: the tenascin family of extracellular matrix proteins; Structural roles: tenascin-X deficiency and Ehlers-Danlos syndrome; Tenascins as modulators of cell adhesion, migration, and growth; Role of tenascin-C in inflammation; Regulation of tenascins by mechanical stress: implications for wound healing and regeneration; Association of tenascin-C with cancer: antibodies as diagnostic and therapeutic tools; Conclusion and perspectives.

show abstract

Tenascin‐C induced stimulation of chondrogenesis is dependent on the presence of the C‐terminal fibrinogen‐like globular domain

Cited by 17 publications

References 17 publications

The Matrikine Tenascin-C Protects Multipotential Stromal Cells/Mesenchymal Stem Cells from Death Cytokines Such as FasL

The Matrikine Tenascin-C Protects Multipotential Stromal Cells/Mesenchymal Stem Cells from Death Cytokines Such as FasL

Role of tenascins in the ECM of gliomas

Tenascins: regulation and putative functions during pathological stress

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